Chapter XLI: Part II: , Showing Predominance of Malarial Element . . . . 617 (40)

The diphtheritic membrane not infrequently spreads from the pharynx to the neighboring organs. From the posterior aspect of the soft palate or pharynx the disease gradually ascends to the nasal cavities; this is particularly apt to occur when the uvula is the seat of extensive deposits, and by forced inspiration and deglutition its posterior surface becomes affected. In such cases the membrane which extends thence to the nasal cavities is very dense, and capable of narrowing the capacity of the nasal cavities anteriorly, and occasionally even to close them entirely; as a rule, however, several days elapse before the membrane assumes such a condition. Usually, when this form of nasal diphtheria is in its incipient stage, it is impossible to diagnosticate it; the most important sign thereof, besides a more nasal articulation and sometimes greater difficulty in deglutition, and the result of close ocular examination while the uvula is turned sideways or drawn forward, is a swelling of the deep facial glands at the angle of the lower jaw; when these swell rapidly it can be asserted positively that the nasal cavities have been invaded. There is little or no discharge from the nostrils under these circumstances.

The picture is a very different one, however, when the nose becomes primarily affected. This usually occurs only where an acute catarrh with but little secretion, not so often where a chronic catarrh, has preceded infection. When the secretion is thin and serous, the diphtheritic infection renders it no thicker, but makes it slightly flocculent, and it may become very profuse. This form is frequently attended with a disagreeable odor, equally unpleasant to the patient and to those around him. During the prevalence of an epidemic one must always be prepared to see an acute nasal catarrh or an influenza, or even a chronic nasal catarrh, become complicated with diphtheria or pass into it. Schuller reports the case of a five-weeks-old male child who, having had a nasal catarrh since birth, became affected with diphtheria of the nose. The glandular {670} swelling of which I spoke above is a very important diagnostic, and likewise a decidedly unpleasant symptom, which becomes very marked inside of twenty-four hours; frequently a partial swelling remains long after the disappearance of the diphtheritic membrane. Such glands rarely suppurate or undergo a necrotic degeneration; sometimes they become permanently indurated. This induration and a chronic pharyngeal and nasal catarrh are very serious matters in many instances. Both of these conditions are starting-points for a number of acute or subacute attacks of diphtheria in the same person. It is they which constitute the liability of persons once affected to be taken sick again. Not only are they liable to be affected themselves, but they are a constant danger to all around them. Diphtheria, in a large family of children living in one of the best houses of the city, after having returned half a dozen times in the course of a year, disappeared instantaneously, not to return, when a seamstress living in an infected neighborhood and suffering from occasional sore throats was relieved of her daily work in the house. Oedematous swelling of the mucous membrane and submucous tissue is often observed for a long period to come; elongated uvulæ, enlarged tonsils, often date back to such an acute attack. Thus it is with the upper portion of the larynx about the posterior insertion of the vocal cords (see below); its large amount of loose submucous tissue is liable to swell considerably in acute attacks. Frequent spells of croupy cough and a certain degree of dyspnoea are often observed for years afterward. Though the cases of genuine cicatrization between the arytenoid cartilages, as described by Michael,[10] be rare, with their result of permanent paresis of the thyroarytenoid interni muscles, when they do occur they are either obstinate or altogether incurable.

[Footnote 10: _Deutsch. Arch. f. klin. Med._, 1879, xxiv. p. 618.]

Diphtheritic conjunctivitis occurs either primarily or as a complication of pharyngeal or nasal diphtheria. Fortunately, it is not of frequent occurrence; the cornea may become destroyed either by pressure through the considerable swelling of the eyelid or by diphtheritic keratitis. Usually the upper eyelid is the first to suffer; it is red, rigid, swollen. In the beginning the conjunctiva palpebræ is smooth, dry and pale, while that of the eye is chemosed; afterward diphtheritic deposits take place either in floccules or in solid masses. Knapp distinguishes between croup and diphtheria of the eyelid according to the facility or impossibility of removing the deposit. In favorable cases the membranes begin to macerate and the eyelids to soften after a few days. In those less favorable perforation of the cornea, prolapse of the iris, or total destruction of the eye take place.

The ear is but rarely the primary seat of diphtheria. A girl of three years died of laryngeal diphtheria on Sept. 6, 1882, after an illness of four days. A girl of seven years was removed from the house on Sept. 6th and returned on Sept. 8th. On the afternoon of the 10th an earring taken from the corpse was attached to the left ear of the sister, after having been washed with soap and water only. About noon on the 11th the lobe of the left ear reddened, on the 12th it exhibited a membrane and became swollen, and some glands enlarged in the neighborhood. On the right mastoid process the skin was not quite healthy, a vesicatory having been applied three weeks previously. This surface became {671} diphtheritic on the 12th, without consecutive glandular swelling. On the 13th the membranes grew thicker; on the 14th the pharynx was also affected, and the physician called in.

Most diphtheritic affections of the ear, however, are secondary. In pharyngeal and nasal diphtheria the narrow orifice of the Eustachian tube is easily obstructed by either catarrhal swelling or diphtheritic deposit. The disease may invade the middle ear and the drum membrane with perforation, caries, and deafness following.

The descent of the diphtheritic process into the respiratory organs may give rise to various conditions. The membrane is not always found to pass uninterruptedly from the mucous membrane of the fauces into the larynx; not infrequently isolated diphtheritic spots are found in the pouches on either side of the attached extremity of the epiglottis, or on the epiglottis, or in the larynx. At such times the epiglottis is moderately swollen, its margins hard and reddened. Occasionally the redness is interrupted by small diphtheritic deposits, which may remain isolated for a considerable time, but generally coalesce so as to coat the edges of the epiglottis with a continuous membrane. As a rule, the upper surface of the epiglottis is not completely covered by membrane, while only now and then diphtheritic deposits are found on its under surface.

The subjective symptoms accompanying the affection of the epiglottis are not always in direct proportion to the extent of the membranes. Dyspnoea and hoarseness occasionally occur where the only abnormal condition is a marked oedema at the entrance of the larynx, particularly of the posterior wall near the arytenoid cartilages and the attachment of the vocal cords. The oedematous condition causes a functional paralysis of the vocal cords, together with marked dyspnoea on inspiration. The difficulty of breathing may become so excessive that the clinical diagnosis of croup is unquestionable, and tracheotomy resorted to, while expiration is comparatively free and the voice not markedly affected. Furthermore, cases occur in which there is no marked oedema, but merely a general catarrh of the epiglottis and larynx; here, too, the subjective symptoms of hoarseness and dyspnoea may become severe and necessitate the performance of tracheotomy. Still, bearing this in mind, I have on several occasions refrained from performing this operation where I judged that, aside from the diphtheria of the pharynx, I had to deal with a moderate oedema of the glottis or a laryngeal catarrh.

Frequently, however, membranes form in the larynx in the same way as in the pharynx or nose; then inspiration and expiration are equally interfered with, and hoarseness is a more constant symptom than in the above-mentioned cases. Fever and pain are not necessarily prominent symptoms; in fact, they are frequently unimportant, but in proportion as the degree of narrowing of the larynx increases the respiration becomes more difficult, long-drawn, and loud.

It may happen that the trachea and bronchi may become affected, although diphtheria of the fauces does not exist. This does not occur as rarely as Henoch and Oertel seem to believe. They think that diphtheritic tracheo-bronchitis is mistaken for the primary condition, because the throat is not examined early enough.

Oertel is of the opinion that the membrane in the fauces is {672} overlooked in such cases. Steiner,[11] too, asserts that "the tendency of the times is to question, nay, rather to deny, the existence of croup extending from below upward." Now, on the contrary, repeated experience enables me to assert with positiveness that diphtheritic tracheo-bronchitis may occur without an affection of the pharynx at the same time. I do not deny that it may last for days without giving rise to dangerous symptoms. I know it does. But when the process reaches the larynx, the symptoms of suffocation become so urgent that tracheotomy may be absolutely required at once, and, in spite of the operation, death soon after occurs.

[Footnote 11: _Ziemssen's Handb._, iv., 1, 126.]

Of course these cases are exceptions; as a rule, laryngeal and tracheal diphtheria result from a descent of the disease from the fauces. More or less uncomplicated cases of primary laryngeal diphtheria, or so-called sporadic membranous croup, were, however, observed before the end of the sixth decade of this century. They were then almost the only cases of diphtheria, and linked former epidemics and the present one together.

Inflammatory affections of the lungs may occur at various times and in various forms during an attack of diphtheria. That which appears after tracheotomy is usually a broncho-pneumonia, and results from rarefaction of the air in the respiratory passages during the period of impeded respiration, with consequent collapse of pulmonary tissue and dilatation of the blood-vessels, and hence a disturbance of the circulation. It may not fully develop until after tracheotomy, and is a frequent cause of death on the second or third day after the operation. Now and then a case of lobular pneumonia will result from the aspiration of pieces of membranes into the smallest bronchi. It can be easily recognized when the trachea is opened, but previous to the operation the auscultatory signs are of little or no value, being masked by the laryngeal râles. Percussion is equally useless, for a dulness may just as well indicate collapse of the lung as infiltration. The second form of pneumonia associated with diphtheria is from the beginning fibrinous in character. Here, too, auscultation and percussion are of little assistance in establishing a diagnosis when there is a laryngeal diphtheria at the same time, for the above reasons. Where, however, the dulness on percussion is accompanied by high fever, and the long-drawn inspiration is replaced by rapid respiratory movements, the diagnosis of pneumonic complication is justified.

Diphtheria of the mouth, as a primary affection, is not of very frequent occurrence; not rarely, however, is it associated with diphtheria of the fauces and nose, mainly when they have assumed a septic or gangrenous character; it appears on cheeks, tongue, angles of the mouth and gums, and, after the fetid discharges have excoriated the skin, on the lips also. In all of these localities it appears less in the form of an extensive, thick membrane than an infiltration of the tissues. It is most apt to occur where, from the start, the mucous membrane of the mouth was eroded or ulcerated. The ulcerated base of a follicular stomatitis is very frequently the starting-point of a general diphtheria of the mouth. It is always a disagreeable symptom, points to a long duration of the whole process, and threatens septic absorption.

The oesophagus and the cardiac portion of the stomach are the seat {673} sometimes of very massive and extensive, mostly fibrinous exudations, in typhoid fever, dysentery, cholera, measles, and scarlatina, or after injuries following contact with mineral acids, alkalies, corrosive sublimate, or antimony. When the normal tissue was not injured I never saw any that were not superjacent and could not easily be peeled off (croupous). In cases of extensive pharyngeal and laryngeal diphtheria the upper part of the oesophagus is often covered to a distance of half an inch or an inch with membrane, the lower part of which is thinning out into a mere film. A case of local diphtheritic deposit near the cardiac portions of the oesophagus, upon the seat of a stricture, I have described in my _Treatise_, p. 83. Actual diphtheria of the stomach is rare. So is that of the intestine, which is much more liable to be affected in animals than in man. In the cow intestinal diphtheria is frequent (Bollinger). In the gall-bladder, resulting from the irritation produced by calculus, it was seen by Weisserfels. The diphtheritic form of inflammation of the human colon and rectum--dysentery--is frequent enough, but will be the subject of discussion in another place. But, besides this, in the lower portion of the small intestines and in the colon long, tough, coherent membranes are sometimes found in the male and female (not in the hysterical female only). As a rule they are not diphtheritic, but consist mostly of nothing but mucus hardened and flattened down by protracted compression. The few cases of intestinal diphtheria I have met with gave rise to the usual symptoms of enteritis, and were diagnosticated as such.

Wounds of all kinds are easily and rapidly infected by diphtheria; for instance, vaginal abrasions and erosions of the external ear, tongue, and corners of the mouth. Scarification or removal of part of the tonsils is followed in half a day or a day by a deposit of diphtheritic membrane on the wound. The wound caused by tracheotomy becomes liable to be infected with diphtheria within twenty-four hours. Leech-bites, skin denuded by vesicatories, removal of the cuticle by scratching during cutaneous eruptions, all furnish a resting-place for diphtheria in a short time. What Billroth has described under the name of muco-salivary diphtheritis, as it occurs after the extirpation of a large portion of the tongue and resection of the lower jaw, belongs to this class.

At times immediately at the beginning of an invasion of diphtheria, at other times only on the second or third day, an erythematous eruption, more or less general, appears on the skin. Now and then it appears on the chest, shoulders, and back; at other times it covers the body, and has not infrequently led to its being confounded with scarlatina. It is not always accompanied by much fever, and cannot therefore be mistaken for that form of erythema which frequently appears in children with delicate skins during high fever from any source. I cannot say that I have found this complication to give a more malignant character to the disease, but true erysipelas does. I am not prepared to prove that the two processes, erysipelas and diphtheria, are identical under some circumstances, but the complication of the two, and the ferocity with which they combine, renders a close relationship probable. I have seen an infant dying from an erysipelas added to a post-auricular diphtheria, this being due to a slight abrasion of the surface. Erysipelas originating in the tracheotomy wound, though ever so carefully disinfected and secured, is {674} frequently observed after two or three days, and is a very ominous symptom. Erysipelatous surfaces, denuded of their epidermis by spontaneous vesication or injured by ever so slight a trauma, are very liable to be covered with diphtheritic membranes.

An eruption resembling urticaria in the beginning is as innocent as erythema, but purpura in the latter stage is a symptom of mostly ominous nature.

On the vulva and vagina of little girls diphtheria is sometimes met with; probably in every case it is due, under the epidemic influence, to a local catarrh or erosion. In but few cases, comparatively, the inguinal glands are swollen. There are not many cases of vaginal diphtheria which are followed by the pharyngeal affection. Diphtheria of the vagina in puerperal women is liable to become the cause of general sepsis, and is a dangerous disease; it is seldom complicated, but uterus, Fallopian tubes, and peritoneum may become the seat of inflammatory and septic disturbances. In the bladder it may occur when the urine is alkaline, in chronic cystitis, after lithotomy, urethotomy, the operation for vesico-vaginal fistula, and in ectopia vesicæ. This form has a marked tendency toward localization, but by extension of the phlegmon, when of putrid character, to the retro-peritoneal cellular tissue, peritonitis may ensue and terminate fatally. Sepsis from absorption is also frequent. Vesical diphtheria is sometimes quite unsuspected. A man of sixty had urinary trouble a long time; his urine was frequently very offensive, containing blood and pus. About five days before his death he suddenly collapsed. I found the bladder well filled, and introduced a catheter, but succeeded in removing but a few drops of fetid liquid. Assuming the presence of a malignant tumor at the neck of the bladder, I attempted to draw off the urine by puncturing above the symphisis pubis; again without success. At the post-mortem examination a thick membranous lining of the bladder was found detached in the form of a sac containing about a quart of urine. During life the beak of the catheter evidently passed into the space between the bladder and the membranous sac, which accounts for the unsuccessful attempts at catheterization.

Diphtheria of the placenta was observed by Schüller. The membrane was between uterus and placenta, and attached to the latter. It resulted from puerperal sepsis. Balano-posthitis is liable to result in local and general diphtheria; so are circumcision wounds. They are apt to become affected either primarily, without apparent cause, or when other members of the family are suffering from the disease.

The kidneys may become affected in various ways. Albuminuria is not always of significance, as it occurs in severe and mild cases alike, both before and after tracheotomy, and therefore is not connected always either with the height of the fever or the degree of dyspnoea; at times it disappears in a few days, in other cases it is of longer duration. It is not invariably complicated with changes in the kidney, neither do we always discover casts or degenerated epithelial cells in the urine. In other respects also it does not behave like albuminuria in scarlatina. In the latter it appears seldom before the second week of the process, and frequently later, while in diphtheria it is often seen early. It sometimes lasts but a few days, particularly in many cases which set in with a high fever, which rapidly diminishes, and terminates in speedy recovery. In {675} these occurrences the presence of albumen appears to attend the rapid elimination of the poison.

Albuminuria seldom lasts longer than a week, and is not often complicated with oedema, but sometimes it is but a symptom of a local or general nephritis, and then hyaline, epithelial, and fibrin casts and granular cells are found in the urine. Nephritis then assumes as serious a character as it possesses in scarlatina. Cases of nephritis, fortunately rare in a very early period of diphtheria, are liable to run a rapid and often fatal course.

The heart and blood are affected in various ways by the diphtheritic process. Where the disease runs a slow course, accompanied by high fever, a granular degeneration occurs, similar to that appearing in other acute infectious disorders--typhoid, for example. In diphtheria, however, it would seem that this condition may arise even without marked elevation of temperature. The pathological changes in the heart produced by diphtheria are not always the same. Ecchymoses, cellular hypertrophy, and granular degeneration have frequently been noticed after death where the symptoms had been severe. The result, of course, is considerable weakness of its muscular tissue, evidenced by the formation of local (Beverly Robinson) thrombi, general sluggishness of the circulation, dyspnoea, muffled heart-sounds, a cool and pale skin, and sudden death, preceded by a very feeble and frequent, sometimes, however, by a very slow, pulse. Aside from this, there is actual endocarditis during the course of diphtheria or convalescence therefrom. It affects especially the valves, and among them particularly the mitral. It is characterized by high fever, precordial pain, attacks of syncope, and a systolic murmur.

The rapid decrease of red blood-cells and a moderate increase of leucocytes were demonstrated by Bouchut and Dubrisay, but the disproportion was not such as to necessitate the diagnosis of leucocythæmia. Wunderlich reports two cases of Hodgkin's disease, the pseudo-leukæmia developing during diphtheria. And the slowness of final recovery in many cases, even of but short duration and not complicated with nervous disorders, appears to point to a serious disintegration of the elements of the blood. The dark color and defective coagulation of the blood in autopsies of diphtheria cases have often been remarked.

The direct and rapid introduction into the blood of a foreign substance has amongst its earliest symptoms fever. This reaction of a nervous system depends both on the quantity and quality of the substance or poison introduced, and on the susceptibility of the patient. High temperatures are, however, not the only, nor are they the most dangerous, nervous symptoms. To the latter belong the different shades of paralysis met with during or subsequent to diphtheria.

Sudden and unexpected collapse is sometimes observed, not infrequently in the earlier part of the disease. The changes found in autopsies, such as a dark color of the blood, deficient coagulability, extravasations into and friability and granular degenerations of the tissues, accumulations of degenerated cells, and granules between the fibres, degeneration mainly of the heart-muscle, the presence of heart-clots, thrombi in remote veins,--they all show to what extent the disease can destroy life in the shortest time possible. In the heart either the pneumogastric or the ganglionic {676} nerves may be affected, and the symptoms will vary accordingly. Paralysis of the former will accelerate the pulse, degeneration of the sympathetic will diminish its frequency, yet death may ensue in either.

The usual form of diphtheritic paralysis makes its appearance during the period of convalescence, at a time when all danger seems to have passed by. As a rule, the soft palate and the muscles of deglutition are the first to be attacked, while the condition of these organs is apparently normal (and no longer oedematous, and thereby inactive, as in the first period of the disease). While they are recovering, or before, the accommodation muscles of the eyes become paralyzed. Sometimes, however, these are the first to be affected. This paralysis does not, as a rule, follow severe cases; on the contrary, it is not uncommon to observe it after apparently mild attacks of the disease. In consequence of the former paralysis, deglutition becomes difficult; fluids are expelled through the nose or enter the larynx and bronchi, thereby giving rise to pneumonia; in the latter there is strabismus. The upper and lower extremities become paralyzed afterward. As a rule, a number of muscles are affected at the same time, and improvement will take place in about the same order in which the individual muscles became affected. After paralysis has become affected, circulation begins to suffer. The extremities now and then become bluish, cool, emaciated; rarely atrophy and fatty degeneration have been observed. The muscles of the neck also become paralyzed; the head cannot be carried, or with difficulty only. The fingers are but seldom affected. The same holds good of the bladder and intestines. The respiratory muscles are not frequently attacked. Their paralysis is very ominous, and may prove fatal in a short time from apnoea.

Not only motory but sensory paralyses may occur. Anaesthesia, amaurosis, deafness have been observed; a number of cases of locomotor ataxia are on record, and but lately Hadthagen[12] publishes a case which he claims as disseminated sclerosis.

[Footnote 12: _Arch. f. Kinderheilk._, vol. v., 1883.]

Sometimes the nervous affection in diphtheria is localized in a peculiar manner; it seems as if there is a predisposition on the part of a certain nerve to become diseased. The case of a boy, active and healthy, in the practice of H. Guleke, is very interesting. In the course of three years he had three attacks of diphtheria. In the very beginning of the disease he always became soporous with an almost normal temperature and a slow but regular pulse. Probably the heart's ganglia are the first to submit to the influence of the poison and exhibit symptoms of flagging function. In most of the cases of diphtheritic paralysis the prognosis is good; the large majority will run a favorable course in from six to ten weeks.

INVASION.--Is diphtheria, primarily, a local or a constitutional disease? Mercado's well-known case of diphtheria, engendered by the biting of a finger, has been alluded to. I know of one case in which the vagina became first affected, and later the pharynx. Bayles saw denuded portions of skin assume a membranous character, and general diphtheria develop afterward. Fresh wounds become diphtheritic, and the general disease arises from this source. Even paralysis will follow. I had a death from diphtheria when a long incision into a phlegmon of the thigh had become diphtheritic. A little girl, who had a considerable amount {677} of discharge from a catarrhal vagina, and sore thighs in consequence, exhibited first, during the epidemic of 1877, membranes on the denuded cutis, and afterward general diphtheria. Brehm reports the case of a woman on whom he performed colotomy. The wound became thoroughly diphtheritic and gangrenous, but the pharynx and respiratory organs remained intact. A few days after, her daughter, who attended her in her sickness, was infected. In her the pharynx was the seat of disorder. Besides, the tonsils are very frequently coated with a membrane without any general symptoms in the beginning, fever and general illness occurring only later on. Now, all of these facts tend to show that there are cases in which the origin of the disease is purely local.

It must, however, not be forgotten that during the prevalence of an epidemic every one is more or less under its influence, and but little is wanting to call forth the disease. Some years ago a well-known physician, with whom I was intimately acquainted, died from facial erysipelas and meningitis which had originated in a slight abrasion of the upper lip. During an epidemic of typhoid we daily see persons with fever, headache, and lassitude. Diarrhoeas are frequent during an epidemic of cholera. An epidemic of diphtheria is accompanied by a great number of cases of pharyngitis. When, in the year 1860,[13] I reported two hundred cases of bonâ fide diphtheria, I at the same time observed one hundred and eighty-five cases of non-membranous inflammations of the throat. Such occurrences may be considered as possible or incipient cases of pharyngeal diphtheria. Therefore, contrary to the view of a local origin of diphtheria, it may be claimed that the individual taking the disease was already saturated with the poison, and the local membrane represented perhaps nothing but a symptom, or at the utmost the causa proxima. Accordingly, then, there are undoubtedly cases in which the pharyngeal membrane is the first cause and symptom of the final affection, and others in which the poisoning of the blood through inhalation is the first step in the development of the disease, amongst the symptoms of which the pharyngeal or nasal membrane counts as one.

[Footnote 13: _Amer. Med. Times._, Aug.]

In these cases the first complaints of the patients relate to their general condition. Sometimes they are ignorant of any local trouble when they consult a physician. When it is perceptible, however, it is usually found on the visible pharyngeal and respiratory mucous membranes. This would seem to indicate that the infectious elements while being inhaled are there deposited. Thus there is a possibility of simultaneous affections of both the throat and the blood in the lungs, in either equal or variable proportions. We are easily led to defend at least a partial admission of the poison by the respiratory act, when we reflect that the membranes which are swallowed are rendered innocuous by the action of the gastric fluids, and, therefore, the alimentary canal, from the oesophagus downward, cannot be made responsible for the admission of the poison into the system. Thus it is that the general symptoms--as fever, lassitude, etc.--precede the local phenomena in very many cases, while there are exceptional cases in which the membrane appears first and the fever later. This is especially the case when the tonsils are very large and occupy a prominent position in the throat.

Those cases which begin with high fever and moderate or no local {678} symptoms must be looked upon as constitutional diseases. If a person, in the course of several hours or a day, be taken with high fever and a moderate membrane-formation, these symptoms subsiding in one or two days, leaving the patient weak and exhausted, but fully restored to health at the end of a week, we would be justified in assuming (cæteris paribus) that there was a rapid absorption of a large amount of poison, and an equally rapid elimination thereof. They are, moreover, the same cases in which the second or third day of the disease furnishes albuminuria, with rapid elimination and speedy recovery. When, however, the process is slow in developing, accompanied by moderate fever, and the course is indolent, we have reason to infer that moderate amounts of the poison are being continually taken into the system and making their influence felt to a moderate degree, but for a longer period. Such are the cases which, without any violent symptoms, are accompanied by frequent local relapses, or run, when the absorption is constant as well as copious, a septic course, or terminate in paralysis.

Thus there are cases in which a local infection of the skin or of a wound may be one of the causes, or the only cause, of the disease, and there are cases in which the poison, in passing through and caught in the pharynx, gives rise to local phenomena before the system at large gives evidence of infection. But, as a general thing, diphtheria must be looked upon as a constitutional disease, giving rise to local phenomena, in the same way as scarlatina does on the skin, on the mucous membrane of the alimentary canal, and in the uriniferous tubules; measles on the skin and respiratory mucous membrane; or typhoid in the lymph-follicles and on the mucous membrane of the intestine; or, in other words, the diphtheritic poison may enter the system locally through a defective, or sore, or wounded integument or through the lungs.

Is diphtheria contagious? Undoubtedly it is. The contagious element is liable to be directly communicated by the patient; it also clings to solid and semi-solid bodies, and in this way is transmitted even after a long time. There is hardly any disease which can cling so tenaciously to dwellings and furniture; it can be transported by the air, though probably not to a great distance, and hence in houses artificially heated, while the windows and doors are mostly closed, rises from the lower to the upper stories; and it is for this reason advisable to keep the sick on the top floor. It is certainly transmitted by spoons, glasses, handkerchiefs, and towels used by the patient. The contagious character increases directly in proportion to the neglect of proper ventilation. That it is spread by the feces is not clearly established in my mind. I can give personally no examples of its being carried by visitors or by the attending physician; this is said to have occurred, however. The character of the disease communicated, and the local manifestation, do not depend on that of the original sufferer; thus mild cases may produce severe ones, and vice versâ, and convalescents can convey the disease in its full force. Naturally, the softer character of the tissues in children renders them more susceptible to infection, and the activity of their lymphatic system more liable to severe forms of the disease.

Many tragic cases are recorded in literature of infection by direct contact from pharynx to pharynx, or from the opening in the trachea to the mouth of the surgeon; and one of the saddest cases, perhaps, is that of {679} the much-lamented Carl Otto Weber. Myself and others have contracted diphtheria from sucking tracheotomy wounds.

In regard to the length of the incubation periods, there can be no better authenticated facts than those contained in a report of Elisha Harris to the National Board of Health, an abstract of which is found in No. 1, _National Board of Health Bulletin_, June 28, 1879. The report says that in the fourth school district of the township of Newark (Northern Vermont), amidst the steep hills where reside a quiet people in comfortable dwellings, the summer term of school opened on the 12th of May. Among the twenty-two little children who assembled in the school-room in the glen were two who had suffered from a mild attack of diphtheria in April, and one of them was, at the time school opened, suffering badly from what appeared to have been a relapse in the form of diphtheritic ophthalmia. Besides, it is proved that these recently sick pupils had not been well cleansed, one of them having on an unwashed garment that she had worn in all her sickness three weeks previously. At the end of the third day of school several of the children were complaining of sore throat, headache, and dizziness, and on the fourth day and evening so many were sick in the same way that the teacher and officers announced the school temporarily closed. By the end of the sixth day from school opening, sixteen of the twenty-two previously healthy children became seriously sick with symptoms of malignant diphtheria, and some were already dying. The teacher and six of the pupils were not attacked, nor have they since suffered from the disease.

A case[14] is reported of a surgeon who, while attending a diphtheritic child, had some secretion thrown into his face. Twelve hours after his right eye was inflamed and painful. The affection proved diphtheritic, and recovery was completed after several weeks only. In a case seen by me, with Dr. L. Bopp, a child removed from a house infected with diphtheria was attacked after fourteen days and eight hours.

[Footnote 14: _Würt. Med. Corresp. Bl._, 1878, No. 2.]

It would then appear that, in the direct communication of the disease to healthy or nearly healthy mucous membranes--as healthy as the prevailing epidemic will allow--the period of incubation is from one or two to fourteen days. In only a small number of cases the disease has an even shorter period of incubation than this, as when tonsillotomy or a similar operation is undertaken during the prevalence of an epidemic. One may rest assured that any operation on the tonsils while an epidemic of diphtheria is at its height will be followed within twenty-four hours by diphtheritic deposits on the wounded part. To what extent we are justified in considering this a bonâ-fide incubation of the disease in a previously healthy body is, of course, another question. It seems to me that these cases positively prove that the operation is only the causâ proxima of a diphtheritic affection, and that we may take it for granted that during an epidemic every individual is more or less under its influence and affected by it, so that it needs but a wound or an accidental abrasion of the surface of the mucous membrane to call the disease into action. In a similar way, fresh wounds or morbid conditions of the mouth may call forth the disease. The ruptured vesicles of a follicular stomatitis are liable to serve as resting-places for diphtheritic membranes, and thus I have seen the complication of a follicular stomatitis with oral diphtheria; and any {680} lacerations of the vagina during labor may become diphtheritic within twenty-four hours. If now, on the one hand, incubation depends on the condition of the affected surface, it is probable, on the other hand, that the intensity of the poison at the time plays an important part in determining the period that is to elapse between infection and the invasion of the disease.

ETIOLOGY.--Diphtheria is pre-eminently a disease of early life; in this respect it is said to differ from the genuine fibrinous bronchitis, which by some is held an absolutely different disease, and stated to occur but rarely in children. But even this statement is probably incorrect. In the spring of 1879 I met with four cases of fibrinous bronchitis in children under three years of age. The number of cases of diphtheria in adult life is not very large, while in old age it is very small. Of 501 deaths in Vienna in 1868, only 1 had reached the age of sixty-two; of more than 300 cases in which I performed tracheotomy but 2 were over thirteen years old.

I do not know that sex exerts any predisposing influence over diphtheria, yet of the six hundred cases or thereabouts of laryngeal diphtheria in which I either personally performed tracheotomy or observed the progress of the disease in the practice of others, I found the majority in males, and the recoveries in inverse proportion to the number thereof, the mortality being greater among boys. As far as age is concerned, nearly all the zymotic diseases are seen most frequently in children. They exhibit a greater disposition to submit to diphtheria than adults, if we except those under ten months. Where, however, the disease has occurred previous to the seventh or eighth month, the greater number of cases has been found under three months. Tigri reports the disease in a child of fourteen days. A child of fifteen days was seen with diphtheritic laryngitis and oesophagitis by Bretonneau, one of seventeen days by Bednar, one of eight by Bouchut, one of seven days by Weikert; Parrot mentions several cases, and Sirédey[15] reports eighteen cases of diphtheria in the newly-born. They occurred in the Hospital Lariboisière in the spring of 1877, and were probably infected by the nurses of a neighboring children's asylum. Membranes were found on the soft palate, tonsils, or larynx, and also on both pharynx and larynx. One case occurred where the posterior nares alone were affected. I have met with four cases of diphtheria of the pharynx and larynx in the newly-born myself. One of these became sick on the ninth day after birth, and died on the thirteenth day; the other died on the sixteenth day after birth; the third was taken when seven days old, and died on the ninth day. The predisposition to diphtheria during childhood[16] seems to be explainable by several circumstances. The mucous membrane of the mouth and pharynx in the child is more succulent and softer, and frequently the seat of a congestive and inflammatory process. The nasal cavities are small and frequently affected by catarrhs, the buccal cavity often the seat of catarrh and of stomatitis, and insufficient cleanliness leads here to irritation of the mucous membrane. Any abnormal state of the mucous membrane, with {681} the exception of an atrophic condition and cicatricial changes, affords an excellent abode for diphtheria. The tonsils are proportionally large; in fact, we rarely see the tonsils in children completely sheltered by the arches of the palate. On the other hand, the pharynx is anything but spacious, and while the protuberant condition of the tonsils affords a resting-place for the invading disease, the remaining space is so small that it becomes a source of uneasiness to the well in many instances, and very much more than that to the child during diphtheritic tumefaction. Furthermore, we must take into consideration the large number and size of the lymphatics, which can be more easily injected in the child than in the adult, according to Sappey, and the fact of greater intercommunication amongst the lymphatics and between them and the system; for S. L. Schenck has found that the network of lymphatics in the skin of the newly-born, at least, are endowed with stomata, loopholes through which the lymph-ducts can communicate with the neighborhood, and vice versâ.[17] These circumstances, although they may have no influence in calling the disease into existence, yet assist in its development and in adding to the severity of the symptoms.

[Footnote 15: Thèse, Paris, 1877.]

[Footnote 16: W. N. Thursfield (_London Lancet_, Aug. 3d, 10th, 17th, 1878) collects 10,000 cases of diphtheria in England between the years 1855 and 1877. Of these 90 per 1000 were under a year, 450 per 1000 from 1-5 years, 260 from 6-10, 90 from 11-15, 50 from 16-25, 35 from 26-45; 25 per 1000 were 45 years and over.]

[Footnote 17: _Mittheil. aus d. Embryol. Instit._, i., 1877.]

On the other hand, while the above reasons go to prove that diphtheria attacks children by preference, there is again an anatomical and physiological condition--to wit, the free slightly acid secretion of the mouth, beginning with the third month--that acts as a hindrance to the frequent occurrence of diphtheria after the third month. A poison or poisonous product of whatever nature can less readily find a hiding-place so long as it can be readily--we might always say must surely be--washed away. During these months of eruptive secretion from the mouth diphtheria, therefore, is not very frequent; thus teething, in the case of diphtheria, cannot be held responsible by mothers fond of diagnosticating dental diseases. In this connection the remark of Krieger ought not to be overlooked, who explains the relative scarcity of the disease in the first year of life by the fact that cumulative influences will produce a great number of cases, and cumulation requires time. Undoubtedly, however, an important etiological consideration is the fact of having had the disease previously. We can cite a host of zymotic diseases the occurrence of which once serves as a protection against future attacks. Not only can no such security be expected after one attack of diphtheria, but, cæteris paribus, the disease shows a preference for those who have survived a previous attack. The statement that only the mild cases, with but slight elevation of temperature and freedom from severe constitutional symptoms, are likely to suffer a relapse is founded on error. True, I have more frequently seen relapses after mild cases--which, fortunately, are in the majority--but the disease has also recurred where originally high fever and an extensive lymphadenitis proved it to be a severe case. Besides, second attacks of membranous croup are also recorded (Guersant, N. F. Gill, Quincke).

As there are individuals, so there are families, which have a predisposition to diseases, as there are others in whom, notwithstanding ample exposure, infection does not easily take place. Yet in the families in which diphtheria is of frequent occurrence it cannot always be attributed to enlarged tonsils and a tendency to pharyngeal or nasal catarrh.

{682} Still, catarrh and the vulnerability of mucous membranes must be considered as a frequent source of diphtheria; children will get numerous relapses often after a nasal or pharyngeal catarrh. Sudden changes in the temperature of the atmosphere or of the surface of the body are therefore dangerous in predisposed persons. And thus it is that while severe epidemics have spared no climate or land known to us, the majority of cases have occurred in winter and spring; in other words, at a time when catarrhal disorders are of most frequent occurrence. In my experience at New York, the first quarter of the year yielded more cases than any other. Still, they are frequent enough in warm seasons. Krieger insists upon the injurious influence of hot summers and dry hot rooms. I do not doubt the correctness of his views, which cannot but be strengthened by the damaging results of our furnace-heating. But the influence of season on the invasion and course of diphtheria is but indirect and conditional, and may be, perhaps, after all, compared with that exerted by filth--a term which is lately used to express all sorts and forms of nastiness, from filthy bodies of men to their clothes, their habits, their food, and the air they breathe, whether polluted by carbonic acid, by excrementitious gases, or by exhalations of sewers.

Cases of diphtheria which are traced to exhalations from sewers (or even to filthy habits of life) are very frequent. Yet typhoid is attributed to the same causes. So is dysentery. Can, then, foul exhalations produce alike diphtheria, typhoid, and dysentery? Do these diseases arise from a common poison? Or is the poison of a treble character, so that a part may give origin to diphtheria, another part to typhoid, a third to dysentery?[18] Have we to deal, in such occurrences, with specific influences, or only with a lowering of the standard of health, thereby affording other morbid influences an opportunity to exercise their power? These questions are still involved in darkness, and constitute problems the solution of which still engages the minds of both individual writers and authorities. A report of the Board of Health of Massachusetts, closely adhering to the results of exact observations,[19] leaves them doubtful, and the affirmative reports of some modern writers do not bear scrutiny.[20]

[Footnote 18: In regard to the causal connection of the two latter diseases with sewer exhalations we can be more positive than in regard to the former.]

[Footnote 19: Author's _Treatise on Diphth._, p. 35.]

[Footnote 20: M. A. Avery, _Med. Jour. and Obst. Rev._, Feb., 1882.]

Air polluted by bad drainage or leaky sewers has been considered responsible for diphtheria as well as for typhoid fever and dysentery. Not only the impairment of general health, but the direct and unmistakable disease, has been attributed to it. Thus Bayley refers, in the endemic of Bromley,[21] the first cases to unventilated sewers and cesspools. School-children multiplied the disease. Thursfield attributes the diphtheria at Ellesmere[22] to the accumulation of excrements under the school-room, and to deficient supply of water, which, moreover, was of bad quality. Tripe (like Railton, Bailey, Russell, Bell) accuses sewer gas;[23] others polluted waters or bad drainage.[24] I have not been convinced, however, that diphtheria can be considered a sewer-gas disease, in the same way as typhoid fever. The deterioration of the general health resulting from the inhalation of foul air is sufficient to explain the outbreak of the individual attack during a prevailing epidemic.

[Footnote 21: _Sanit. Record_, Aug. 10, 1877.]

[Footnote 22: _San. Rec._, 158, 1877.]

[Footnote 23: _Ibid._, June 14, 1878.]

[Footnote 24: _Ibid._, April 18, May 2, 1879.]

{683} In regard to polluted water, I do not think that pathologists who attribute infectious diseases to bacteria only are justified in condemning it. It may not be so guilty, after all, for the admixtures, inorganic and organic, minerals, admixtures of wood and plants, also lower fungi and their products--algæ, infusoria--would render water rather disagreeable, but not exactly unhealthy. The latter effect can be accomplished--always assuming the bacteria theory correct, for the sake of argument--by bacteria only. But when they arrive in the stomach, their doom is sealed; they are decomposed. The only places where, possibly, they could take root would be diseased or ulcerated places in either the oral cavity or the upper portion of the oesophagus.

Not only water, but the milk of animals also, has been accused of being the direct cause of diphtheria. Powers concludes, though a connection between diphtheria and the consumption of milk have not been proven as yet, that it is very probable indeed. His careful investigations into the causes of some local epidemics in North London exclude any other source from which the people could have been affected. Perhaps one of the forms of garget, cow mammitis, is of an infectious character. His reasoning, however, is not accepted by A. Dowrus,[25] who still believes that the milk which gave rise to diphtheria at a distance may have been soiled and infected. For though the connection between milk and scarlatina and typhoid fever had been known for years and variously studied, no observation of the kind had yet been made in regard to diphtheria. Besides, where the young, in England, drink much milk--viz. in the cities--diphtheria was very much less frequent than where little or no milk was taken--viz. in the country. Even in the country the well-to-do classes, who drink milk, had but little diphtheria, while the children of the poor, who obtained none, suffered a great deal from it.

[Footnote 25: "Diphtheria and Milk-Supply," _Brit. Med. Journ._, Feb. 1, 1879.]

In regard to this transmission of diphtheria by means of milk O. Bollinger[26] hesitates to express any opinion, except that the matter is very doubtful indeed. Probably the possibility of contracting diphtheria directly from animals is very much greater than the danger from water or milk. On a Pomeranian farm, during the winter 1875-76, every newly-born calf died of diphtheria. The superintendent of the farm and the woman who attended to the calves were taken with diphtheritic angina.[27] Similar occurrences have been recorded. Bollinger reports a mycotic disease of the trachea and lungs in birds.

[Footnote 26: _D. Z. f. Thiermed. u. vergleich. Pathol._, vi., 1879, p. 7.]

[Footnote 27: Damman, in _D. Zeitsch. f. Thiermed._, 1876, p. 1.]

Friedberger's report,[28] presented to the Veterinary Society of Munich, on croup and diphtheria of domestic fowls, leaves no doubt as to its frequency, particularly amongst the nobler varieties.

[Footnote 28: _D. Zeitsch. f. Thiermed._, v., 1879, p. 16.]

Nicati[29] studied an epidemic diphtheria amongst hens which had similar symptoms and a course very much like that in man; it could be inoculated into other animals, and was contemporaneous with the outbreak of the epidemic amongst the human population of Marseilles. Trasbot[30] succeeded in inoculating a healthy hen from a diphtheritic one, but the {684} attempts at transmission to dog, pig, and man were unsuccessful. The _Med. and Surg. Journal_[31] contains the following: In a house at Ogdensburg, N.Y., five children were ill with diphtheria. Three kittens who had been playing with them from time to time took the disease and died. Post-mortem examination showed diphtheritic membranes in their throats.[32]

[Footnote 29: _Revue d'Hygiène et de Police sanitaire_, 1879, p. 3.]

[Footnote 30: "De la transmission de la Diphth. des Animaux à l'Homme," _Gaz. hebdom._, 1879 Avril 25.]

[Footnote 31: _Med. Rec._, Nov. 8, 1879.]

[Footnote 32: An elaborate description of the croupo-diphtheritic inflammations of mucous membranes in hens, turkeys, pheasants, and pigeons may be found in _Zürn. Krankh. d. Hausgeflügels_, 1882, p. 104.]

Gerhardt[33] reports the following: 2600 hens were imported from Verona, Italy, into a village, Messelhausen, in Baden. Some of these hens were affected with diphtheria when they arrived. Within six weeks 600 of their number died of diphtheria, and 800 more soon after. In the following summer 1000 chickens were raised by artificial breeding, all of which died of diphtheria within six weeks. Five cats kept in the place also died of diphtheria; a parrot fell sick with it, but recovered. An Italian cook, suffering from diphtheria, in the month of November, 1881, while being subjected to local treatment with carbolic acid, bit the head-nurse's left foot and hand. Both these wounds became diphtheritic, the man falling sick with high fever, and requiring three weeks for his gradual recovery. Besides, four of the six workingmen employed in taking care of the hens of the establishment were taken with diphtheria. Not a single case, however, occurred in the neighboring village. Thus, it is safe to assume that the diphtheritic disease of hens can be transmitted to man.

[Footnote 33: _Verhandlungen des_ (ii.) _Congresses für Innere Medicin_, Wiesbaden, 1883, p. 129.]

Diphtheria may be also produced by outside influences. In this regard the attempts at generating pseudo-membranes by artificial means are very interesting indeed. As early as 1826, Bretonneau, by the introduction of tincture of cantharides and olive oil into the trachea, succeeded in producing a "dense, elastic, reed-like membranous concretion." Delafond called croup into existence by the use of ammonia, oxygen, chlorine, corrosive sublimate, arsenic, and sulphuric acid. On the other hand, H. Mayer asserts that it is impossible, by means of ammonia, to produce a croup in the windpipes of animals which in the slightest degree resembles that occurring in human beings. Trendelenburg, however, after producing membranes in the trachea by the use of a solution of corrosive sublimate (1:120), succeeded in hardening the entire mass with bichromate of potassium, which it was impossible to do with the most tenacious mucus.

Rey observed croup in horses that inhaled smoke in a burning stable.[34] In the collection of the veterinary school of Zurich there is a croup membrane from a heifer which had been exposed to a fire; at Munich, one from the trachea of a horse, produced by forcibly injecting medicines into the nose. Hahn made an observation on cows, W. Ammon on horses, of long croup membranes after the animals had been exposed to smoke and fire; and Oertel constantly insists on there being "no actual difference between croup as it ordinarily occurs and that excited in the windpipe of a rabbit by means of ammonia. The color and texture, the physical, chemical, and histological characteristics, are identical."

[Footnote 34: _Journ. de méd. vét. de Lyon_, 1850, p. 249.]